Common Sweetener Ups Obesity Risk Without Warning

The rise in obesity may be linked to common sweeteners found in many foods. Experiments shown that eating too much fructose increases the risk of leptin resistance, a condition that can lead to obesity when paired with a high-fat, high-calorie diet.

The latest findings have been published in the American Journal of Physiology
University of Florida College of Medicine Researchers in Gainesville, who led the experiments, described leptin as a hormone that plays a role in helping the body to balance food intake with energy expenditure, and leptin resistance as a condition when the body stops responding to it.

They highlighted that fact that leptin resistance is associated with weight gain and obesity in the face of a high-fat, high-calorie diet.

Though fructose is found in fruit, the researchers say that the normal consumption of fruit is not problematic.

This study may explain how the global increase in fructose consumption is related to the current obesity epidemic According to them, it is the consumption of table sugar and high-fructose corn syrup, added to many foods these days, which is causing people to eat much more fructose than ever before.

For their study, the researchers fed two groups of rats the same diet over a period of six months, with one important exception: one group consumed a lot of fructose while the other received no fructose.

During the six months, there were no differences in food intake, body weight, and body fat between rats on the high-fructose and the rats on the fructose-free diets. There was also as no difference between the two groups in the levels of leptin, glucose, cholesterol or insulin found in their blood.

The only difference observed at the end of the six months was that the rats on the high-fructose diet had higher levels of triglycerides in their blood.

In order to find out whether the animals had become leptin resistant, the researchers injected them with the hormone: the rats whose leptin response was functioning normally would lower their food intake.

The team observed that the rats on the high-fructose diet had become leptin resistant, as they did not lower their food intake when given leptin.

This first six months of the study showed that leptin resistance can develop silently.
"Usually, leptin resistance is associated with obesity, but in this case, leptin resistance developed without obesity. This was very surprising," said Alexandra Shapiro, a member of the research team.

"This study may explain how the global increase in fructose consumption is related to the current obesity epidemic," Shapiro said.

The researchers plan to study in their future research whether leptin resistance can be reversed by removing or reducing the fructose content of the diet.

Further experiments showed that the leptin resistant rats ate more and gained much more weight and fat than the leptin responsive animals on the fructose-free diet.